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64 Cards in this Set
- Front
- Back
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What is margination of leukocytes
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Accumulation of leukocytes along the endothelial surface.
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What mediates margination?
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Mechanical and chemical mediators
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What are the chemical mediators that mediate leukocyte margination?
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C5a, leukotriene B4 and bacterial products
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Rolling, adhesion and transmigration of leukocytes is mediated by what?
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Binding of complementary adhesion molecules on leukocytes and endothelial surfaces
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What are the adhesion molecules involved in leukocyte Rolling, adhesion and transmigration?
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Selectins, integrins, immunoglobulins, mucin like glycoproteins.
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What is the role of E- selectin and P-selectin in leukocyte rolling?
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E-selcetin and P-selection are present on endothelial surface. They bind to sialyl-lewis X on leukocytes
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What are the levels of selectins in the normal endothelium? During inflammation?
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They are present in very low levels. During inflammation they increase in number after stimulation by specific mediator (histamine, thrombin)
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Where is P-selectin stored?
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Weibel palade bodies
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What occurs to the distribution of P-selectin upon the activation of histamine and thrombin?
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P-selectin is redistributed to the cell surface
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What increases the expression of endothelial adhesion molecules ICAM-1 and VCAM-1 ?
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Cytokines TNF and IL-1
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What activates leukocytes to increase binding affinity of integrins?
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C5a and LTB4
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What do integrins bind to in the endothelial surface?
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ICAM-1 and VCAM-1
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What mediates the transmigration of leukocytes ?
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Interaction of platelet endothelial cell adhesion molecule 1 (PECAM –1) Neutrophils release type IV collagen that degrades the basement membrane
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What is chemotaxis?
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The attraction of cells toward a chemical mediator that is released in the areas of inflammation
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What are the important exogenous chemotactic factors Neutrophils?
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Bacterial products, such as N-formyl methionine
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What are the important exogenous chemotactic factors for Neutrophils?
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Leukotrine B4 (LT-B4), complement system products C5a. alpha chemokines (IL-8)
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What is phagocytosis?
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Engulfment of particulate material bu phagocytic cells
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What are the most imp. Phagocytic cells?
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Neutrophils and macrophages
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What are the 3 steps of phagocytosis?
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Recognition and attachment. Engulfment. Killing and degradation of the ingested material
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What is opsonization?
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It facilitates phagocytosis, coating of particulate matter by substances referred to as opsonins
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What are the 3 important opsonins?
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IgG, C3b and collectins
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What triggers the engulfment by phagocytes?
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Binding of opsonised particle to phagocytic receptor
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After binding of opsonized particle to phagocytic receptor what occurs next?
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Neutrophils send out cytoplasmuc processes that surround bacteria
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What is a phagolysosome?
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Phagosome fuses with lysosome to form phagolysosome
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What is degranulation?
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Release of lysosomal contents
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What is the final step in phagocytosis of microbes?
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Killing and degradation
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What is the most efficient bactericidal system in Neutrophils?
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Oxygen dependent killing
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What is the first step that occurs in oxygen dependent killing after phagocytosis has occurred
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NADPH oxidase converts molecular oxygen in superoxide free radical in the presence of NADPH. Energy given off in this reaction is called respiratory burst
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What mediates the less effective oxygen independent killing by Neutrophils
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Substances in leukocyte granules; such as lysozyme, lactoferrin, major basic proteins, bacterial permeability increasing protein, defensins
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What us responsible for the degradation of dead organisms?
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Lysosomal acid hydrolases
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What is a neutrophil?
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Polymorphonuclear leuokocytes – key cell in acute inflammation
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What receptors are present in a neutrophil,
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IgG and C3b
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What are the contents of a primary neutrophil granule?
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Myeloperoxidase, phospholipase A2, lysozyme, acid hydrolases, elastases, defensins, bacterial permeability increasing protein.
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What are the contents of secondary granules?
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Phospholipase A2, lysozyme, leukocyte alkaline phosphatase, collagenase, lactoferrin, vitamin B12 binding proteins.
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What is the main inflammatory cell in acute inflammation?
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Neutrophils come to the site of injury within the first 24 h
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What cells arrive at the site of injurt 2-3 days after injury occurs?
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Monocytes-macriphages lymphocytes
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What is chronic granulomatous disease of childhood?
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X –linked Recessive disease. Characterized by absence of NADPH oxidase activity. Marked by phagocytic cell that ingest but not kill certain microorgs.
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What are some of the characteristics of myeloperoxidase deficiency?
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Autosomal recessive, infections with candida, usually little clinical consequence
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What is chediak-Higashi syndrome?
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AR disease, characterized by: neutropenia, albinism, cranial and peripheral neuropathy and a tendency to develop repeated infections. Presence of ab. leukocytes
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What is defective in leukocyte adhesion deficiency type 1?
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Defective synthesis of integrins LAF-1 and MAC –1. recurrent bacterial infections
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What is defective in leukocyte adhesion deficiency type 2?
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Absence of sialyl lewis X on Neutrophils. Recurrent bacterial infections
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What steps are involved in the exit of neutrophils from the blood into tissues?
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There are three steps: (1) In the vessel lumen: margination, rolling, and firm adhesion; (2) transmigration across the endothelium; and (3) migration in interstitial tissue toward a chemotactic stimulus
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What adhesion molecules are relevant for emigration of inflammatory cells?
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1) Selectins: E-selectin and P-selectin on endothelium and L-selectin on neutrophils; P- and E-selectins bind to sialyl Lewis X on the neutrophils, and L-selectin to mucin-like molecules on endothelium; (2) Immunoglobulin family molecules: ICAM-1 and VCAM-1 on endothelium bind to integrins (eg, LFA-1, Mac-1, and VLA-4) on leukocytes.
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At what stages do they function?
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Selectins are involved in rolling. Integrins are involved in firm adhesion. PECAM-1, another adhesion molecule expressed on both leukocytes and endothelial cells, is involved in transmigration.
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What mechanisms do neutrophils use to kill microbes?
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Two mechanisms are used: (1) oxygen-dependent and (2) oxygen-independent. Oxygen-dependent mechanisms are the most important. They involve generation of superoxide O2- via the NADPH system. This gives rise eventually to H2O2 and OH-. Also generated are myeloperoxidase-dependent HOCl- radicals. Oxygen-independent mechanisms include lysozyme, lactoferrin, and defensins
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Do you know of any defects in neutrophil killing mechanisms?
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Three important defects are (1) defects in adhesion due to genetic deficiency of B2 integrins (LAD-1); (2) defects in chemotaxis or phagocytosis from an inherited impairment in assembly of microtubules (eg, Chediak-Higashi syndrome); (3) defects in microbicidal activity due to a genetic deficiency of the NADPH oxidase system (called chronic granulomatous disease) or genetic deficiency of myeloperoxidase.
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What is acute salpingitis?
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Acute inflammation of fallopian tubes
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What are some examples of harmful effects of repair?
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Formation of scars, disfigurement, intestinal obstruction.
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What are some of the characteristics of acute inflammation?
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Early response to injury, infection chemical agents. Rapid onset, short duration, exudation, accumulation of neutrophils
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What are some of the characteristics that help distinguish from acute and chronic inflammation?
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Longer duration, influx of lymphocytes and macrophages
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Exudation
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The escape of fluid, proteins and blood cells from the vascular system into the interstitial tissue or body cavities.
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Exudate
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An inflammatory extravascular fluid with a high protein concentration. Implies sig. Alteration in permeability of small blood vessels inan area of injury
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Transudate
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Extravascular fluid with a low protein content few or no cells. Results due imbalence in hydrostatic pressure.
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Edema
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Excess amount of fluis in interstitial spaces or body cavities. Can be exudates or transudate
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Pus
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Purulent exudates is inflammatory rich in neutrophil and debris of dead cells
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What is the purpose of inflammation?
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To get Neutrophils to the site of injury. To celar the invading organism and begin the process of healing
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What are the 5 cardinal signs of acute inflammation?
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Calor, rubor, tumor, dolor, functio laesa
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What is the mechanism of calor in inflammation?
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Heat- histamine dependent vasodilation
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What is the mechanism of rubor in inflammation?
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Redness- histamine dependent vasodialtion
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What is the mechanism of tumor in inflammation?
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Swelling- histamine dependent increase in vascular permeability
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What is the mechanism of doloe in inflammation?
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Pain- due to prostaglandin E2 and bradykinin
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What causes the vasodilation in inflammation?
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Mast cells release histamine which acts on vascular smooth muscle cells.
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What causes the increase in permeability of venules in inflammation?
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Histamine contracts endothelial cells, causing movemnt of fluid into interstitial tissue.
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What causes stasis in inflammation?
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The outflow of fluid form the blood vessels‡ increase viscosity. Rouleau formation, alteration in lamina flow, neutrophil margination
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